Overhydration, underhydration, and total body sodium: A tricky "ménage a trois" in dialysis patients.

Overhydration is a frequent complication in dialysis patients. It has been linked with hypertension, left ventricular hypertrophy, arterial stiffness, atherosclerosis uremic cardiomyopathy, and all-cause mortality or cardiovascular morbidity. In addition, predialysis underhydration is also associated with increased risk of death in ESRD patients. In this context, the optimal evaluation of hydration status is a must. However, this mission is not easy or accurate. In the last 10 years, several new methods have been tested in dialysis patients, particularly bioimpedance and lung ultrasonography. The precise clinical value of these techniques in the daily care of hemodialysis patients is not obvious yet. Sodium is also an important piece of this puzzle. Salt intake and/or removal of sodium during dialysis are essential determinants of optimal hydration status. Recent studies have revealed that salt and water homeostasis is also dependent of tissue sodium storage-increased in hemodialysis patients. However, the significance of increased sodium tissue storage as a cardiovascular risk factor and the relationship between tissue sodium content and hard CV endpoint have not yet been elucidated yet.

[Hyperhydration and dialysis in acute kidney failure]. / Überwässerung und Dialyse beim akuten Nierenversagen.

Despite the advances in critical care medicine, the hospital mortality in patients with acute kidney injury (AKI) requiring dialysis remains high. Depending on the underlying disease the in-house mortality is reported to be up to 80%. Several observational studies demonstrated an association between mortality and fluid overload. A primary mechanism of interest is that fluid overload causes tissue edema and subsequent reduction of perfusion, oxygenation and nutrient delivery. This results in further renal damage. In addition, fluid overload-related dilution within the extracellular space causes artificially low serum creatinine, which masks AKI diagnosis. As a consequence, renal protective management strategies are deferred, which further aggravates kidney injury. This aggravation of renal damage subsequently increases the mortality. This review discusses the role of fluid overload for outcomes in critically ill patients as described in the current literature and assesses criteria for the initiation of renal replacement therapy in this critically ill population.

Fatal water intoxication and cardiac arrest in runners during marathons: prevention and treatment based on validated clinical paradigms.

Cerebral edema due to exercise-associated hyponatremia and cardiac arrest due to atherosclerotic heart disease cause rare marathon-related fatalities in young female and middle-aged male runners, respectively. Studies in asymptomatic middle-aged male physician-runners during races identified inflammation due to skeletal muscle injury after glycogen depletion as the shared underlying cause. Nonosmotic secretion of arginine vasopressin as a neuroendocrine stress response to rhabdomyolysis mediates hyponatremia as a variant of the syndrome of inappropriate antidiuretic hormone secretion. Fatal hyponatremic encephalopathy in young female runners was curtailed using emergent infusion of intravenous hypertonic (3%) saline to reverse cerebral edema on the basis of this paradigm. This treatment was arrived at through a consensus process within the medical community. An increasing frequency of cardiac arrest and sudden death has been identified in middle-aged male runners in 2 studies since the year 2000. Same-aged asymptomatic male physician-runners showed post-race elevations in interleukin-6 and C-reactive protein, biomarkers that predict acute cardiac events in healthy persons. Hypercoagulability with in vivo platelet activation and release of cardiac troponin and N-terminal pro-brain natriuretic peptide were also observed post-race in these same subjects. High short-term risk for atherothrombosis during races as shown by stratification of biomarkers in asymptomatic men may render nonobstructive coronary atherosclerotic plaques vulnerable to rupture. Pre-race aspirin use in this high-risk subgroup is prudent according to conclusive evidence for preventing first acute myocardial infarctions in same-aged healthy male physicians. On the basis of validated clinical paradigms, taking a low-dose aspirin before a marathon and drinking to thirst during the race may avert preventable deaths in susceptible runners.

[Fatal aspiration following polydipsia in schizophrenia]. / Polydipsie bei paranoider schizophrenie mit tödlichem ausgang.

OBJECTIVE AND METHODS: Polydipsia with hyponatraemia commonly occurs with chronic psychosis and is associated with a reduced life expectancy for individuals diagnosed with schizophrenia. We describe a 51 years old man who presented with polydipsia during a relapse of paranoid schizophrenia. While treated with Clozapine, and despite regular observation and daily control of creatinine and electrolytes, the man suddenly collapsed and died after drinking huge amounts of water. No sedation from psychotropic medication or drugs and alcohol was present in this case. Sodium levels on the day of death and the day before were within normal range. A post-mortem revealed aspiration of water and gastric content as the cause of asphyxiation and death. A literature search in Medline and Embase did not yield a description of a similar case. RESULTS AND CONCLUSIONS: This case highlights the risk of aspiration associated with polydipsia in chronic schizophrenia. Daily control of electrolytes to identify hyponatremia and regular observation are recommended but may not be sufficient to prevent sudden death from drinking huge amounts of water.

Fluid overload and acute renal failure in pediatric stem cell transplant patients.

Acute renal failure (ARF) with fluid overload (FO) occurs often in stem cell transplant (SCT) recipients. We have previously demonstrated that an increased percentage of FO prior to the initiation of continuous renal replacement therapy (CRRT) is associated with mortality in children with ARF. Based on these data, we devised a protocol for the prevention of FO in SCT patients with ARF. SCT patients with ARF and 5% FO were started on furosemide and low-dose dopamine. To allow for nutrition, medication, and blood product administration, RRT was initiated for patients with > or =10% FO. There were 272 patients who received allogeneic SCT from 1999 to 2002. Of these, medical records of 26 SCT patients with a first episode of oliguric ARF were reviewed. The mean patient age was 13+/-5 years (range 2-23.5 years). Mean days to ARF after SCT were 28+/-29 days (range 2-90 days). Of the 26 patients, 11 (42%) survived an initial ARF episode. All 11 survivors either maintained <10% FO during their course or re-attained <10% FO with RRT treatment. Of the 15 non-survivors, 6 had <10% FO at the time of death. Of 14 patients who received RRT, 4 (29%) survived. Mechanical ventilation and pediatric risk of mortality score > or =10 at the time of admission to the intensive care unit were associated with lower survival ( P<0.05). The use of one or more pressors, the presence of graft-versus-host disease, and septic shock were not correlated with survival. Our data demonstrate that maintenance of euvolemia ( <10% FO) is critical but not sufficient for survival in SCT patients with ARF, as all non-euvolemic patients died. We suggest that aggressive use of diuretics and early initiation of RRT to prevent worsening of FO may improve the survival of SCT patients.

Fatal self-induced water intoxication among schizophrenic inpatients.

Between 1986 and 1998, a review of 61 records of patients who died before the age of 53 years in eight psychiatric departments whose catchment area had a total population of 559,429 inhabitants revealed that 24 (39.3%) of those patients had a schizophrenic disorder. Of those 24 patients, one (4.17%; 95% CI: 0-21%) died from complications of self-induced water intoxication (SIWIS). Among the 37 remaining patients, two (5.4%; 95% CI: 0-18%) died from complications of SIWIS.

Death by water intoxication.

With recent emphasis on increased water intake during exercise for the prevention of dehydration and exertional heat illness, there has been an increase in cases of hyponatremia related to excessive water intake. This article reviews several recent military cases and three deaths that have occurred as a result of overhydration, with resultant hyponatremia and cerebral edema. All of these cases are associated with more than 5 L (usually 10-20 L) of water intake during a period of a few hours. The importance of maintaining adequate hydration in exertional heat illness prevention cannot be overemphasized, but excessive fluid intake may lead to life-threatening hyponatremia. Current guidelines provide safety by limiting fluid intake during times of heavy sweating to 1 to 1.5 L per hour.

Death from self-induced water intoxication among patients with schizophrenic disorders.

Review of 60 consecutive records of patients who died before the age of 53 years in a state mental hospital revealed that 27 of those patients (45%) had a schizophrenic disorder. Of those 27 patients, five (18.5%) died of the complications of self-induced water intoxication and schizophrenic disorders (SIWIS). Clinical, laboratory, and autopsy features of those five SIWIS patients and of an additional five SIWIS cases obtained from the literature include psychosis, polydipsia, polyuria, severe hyposthenuria (specific gravity 1.003 or less), hyponatremia, seizures, coma, and cerebral and visceral edema. SIWIS characteristically develops during Arieti's third or "preterminal" stage (5 to 15 years after onset of psychosis) of schizophrenic disorders and it must be included in the differential diagnosis of unexplained death among psychiatric patients. As there are no pathognomonic SIWIS tissue changes, the pathologist must carefully integrate clinical, laboratory, and autopsy findings to arrive at the proper diagnosis. When premortem findings of polydipsia and hyponatremia are not available, evidence of antecedent severe hyposthenuria and postmortem vitreous humor hyponatremia of less than 120 mEq/1 are strongly supportive of the diagnosis of death due to SIWIS.

Fatal compulsive water drinking.

In two cases of psychogenic polydipsia, water intoxication developed and contributed to the patient's death. The treatment of the patient with psychogenic polydipsia has been based on the presumed reversibility of the condition. Treatment of such patients must be reconsidered in light of these deaths.

Water intoxication death following hypothalamic lesions in the rat.

Rats received large, bilateral lesions of the ventromedial hypothalamus. Water or saline intakes, urine outputs and body temperatures were observed for up to 24 hr after surgery. Fifty percent of the operated animals drank excessively and died within 4-6 hr when permitted access to water. Urine outputs were low and symptoms of water intoxication were evident. When allowed access to saline, outputs rose and the number of animals which survived increased as the saline concentration increased. Body temperatures approached 40 degrees C during drinking, but did not differ from operated animals which refused to drink. It was concluded that the deposition of metallic ions strongly stimulates a hypothalamic drinking system which results in overhydration and water intoxication death.